J. clin. Path. (1965), 18, 729

Phycomycosis of the bronchusR. M. WINSTON

From Hope Hospital, Salford, Lancashire

SYNOPSIS A case of phycomycosis of the bronchus in a 29-year-old diabetic man is reported.The interval between infection and death was not less than 35 days. Infection of the bronchusappears to have been direct. The diagnosis of phycomycosis could have been made before death.

Phycomycosis is rare; references to all the reportedcases have been given by Symmers (1962), Baker,Seabury, and Schneidau (1962), La Touche, Suther-land, and Telling (1963), Burkitt, Wilson, and Jeliffe(1964), and Mukerji (1964), but is probably morecommon than the few reports suggest (Symmers,1962). Four cases have been reported in the UnitedKingdom, one from Worcester (Kurrein, 1954),two from London (Symmers, 1962), and one fromLeeds (La Touche et al., 1963). A fifth case fromthe United Kingdom is reported in this article.

CASE REPORT

The patient, an Irishman aged 29, lodged in Stretfordnear Manchester. In January 1963, according to hislandlord, he began to be nervy and breathless. Hishealth steadily deteriorated and he was admitted tohospital on 9 May 1963. Diabetes mellitus with markedketosis was diagnosed and rapidly controlled and otherabnormalities were investigated and treated concurrently.Twenty-two teeth were extracted on account of pyor-rhoea. A severe stomatitis yielded Candida albicans onculture and cleared with oral nystatin. A radiograph ofthe chest on 10 May showed some increase in the sizeof the right hilar shadow with slightly increased shadow-ing extending into the right lung field, and this picturewas unchanged six days later. No acid-fast bacilli werefound in six specimens of sputa and two of faeces. Twosputa were negative for tuberculosis on culture. Broncho-scopy was performed on 27 May and the right mainbronchus was found to be partly blocked by what lookedlike sloughing mucosa. A portion of this slough wasremoved and reported to be a grey, sludge-like materialwith many small islands of pus cells, together with sometissue fragments covered by regular squamous or pseudo-stratified epithelium. The deeper tissues showed heavyinfiltration with mixed inflammatory cells and werecongested. Greatly improved in health and stabilized onmorning and evening doses of insulin, he was dischargedfrom hospital on 4 June. There is some doubt whether hecontinued to take both daily doses but his health remainedgood. On 13 June 1963 he died suddenly; his death was

Received for publication 23 March 1965.

reported to H.M. Coroner, and the body was refrigeratedand a post-mortem examination made 22 hours afterdeath.Death was clearly due to haemorrhage from a lesion of

the right main bronchus and adjacent pulmonary artery.No abnormalities other than this local lesion and haemor-rhage were found. The right main bronchus was almostcompletely blocked by a soft greyish-purple mass. Onsection an approximately spherical, unencapsulated mass,approximately 14 cm. in diameter, was found infiltratingthe bronchus and pulmonary artery. No cultures wereprepared.

Microscopy showed that the lesion seen at necropsywas an ischaemic infarct of the bronchus and pulmonaryartery surrounded by a narrow zone of polymorphinfiltration, surrounded in turn by a broad zone of morechronic inflammation. Rupture had occurred at the edgeof the infarct and here there was some fibrosis. Hyphaewere plentiful in the infarct (Figs. 1 to 3) and in the zoneof polymorph infiltration. They were thin-walled, rarelyseptate and irregular, varying in diameter from 2 t to24g. Branching was irregular. Contrast was excellentwith iron haematoxylin but poor with alum haematoxylin.The hyphae were periodic-acid-Schiff and Gram-negative and did not stain with silver. Vascular invasionwas prominent in the infarct and nerve was infiltrated,but cartilage was not invaded. In contrast to the infarct,hyphae were very scanty in the broad zone of morechronic inflammation and were found only as smallfragments in granulomas. These consisted of a small,central mass of pus surrounded by epithelioid cells andgiant cells and hyphae were found in the pus, among theepithelioid cells (Fig. 4) and in the giant cells. Lung andbronchial lymph nodes were included in the tissuesexamined. There was a mild inflammatory reaction in thelung but little reaction in the lymph nodes. No hyphaewere found in the lung and there was no infiltration oflymphatics or lymph nodes by hyphae.

In view of these findings the tissue removed at broncho-scopy was reviewed and the original histological reportwas confirmed. The surgeon had apparently removedinflamed bronchus adjacent to the infarct. The paraffinblock was then serially sectioned and deep in it a tinyfragment of necrotic tissue was found infiltrated byhyphae identical with the hyphae found at necropsy(Fig. 5). Also, a dense mycelium was found in pus in the

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FIG. 1. Bronchial infarct withtypical phycomycete hyphae. Ironhaematoxylin and eosin x 400.

FIG. 2. Bronchial infarct withtypical phycomycete hyphae. Ironhaematoxylin and eosin x 400.

FIG. 3. Phycomycete infiltratingan infarcted blood vessel. Ironhaematoxylin and eosin x 100.

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Phycomycosis of the bronchus

FIG. 4. Hvpha among epitheloid cells. Iron hiand eosin x 400.

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FIG. 5. Phycomycete in bronchial tissue rem

life. Iron haematoxylin and eosin x 400.

bronchial lumen. The hyphae forming thrresembled those found in the infarct, excepwere narrower and septate, though, on exammagnification of x 1,250, many of the septaeto be false and due to collapse and folding.No fruiting bodies were found in 163 sezti

COMMENT

The fungus other than the dense myceliur

the bronchial lumen is identified as a phycomycetebecause it fits the criteria given by Emmons, Binford,and Utz (1963). More detailed identification is im-possible in the absence of fruiting bodies. It isconsidered to be a pathogen and not a post-morteminvader because hyphae were found in granulomasaround the infarct and in giant cells. The associationof phycomycosis with diabetes mellitus is wellknown and needs no comment.How this patient came to be infected is not known.

He was not infected by his surgeon, because thecharacteristic hyphae were found in the tissue re-moved at bronchoscopy. This tissue and the chestradiograph taken on the day after admission tohospital strongly suggest that he was infected be-

!aematoxylin fore admission, and therefore the interval between in-fection and death cannot have been less than 35 days.The histological findings in this case are those of

visceral phycomycosis and not those of the dermaltype. However, it cannot be classified with any ofthe three main clinical types of the visceral disease

M j - pulmonary, rhinocerebral, and alimentary. In thepulmonary type it is assumed that infection is causedby inhalation of spores and bronchial involvementoccurs by direct extension of a lung lesion. In thecase described here no evidence of any pre-existinglesion of lung or bronchus was found and infectionof the bronchus appears to have been direct.

In a section taken through the edge of the ruptureof the pulmonary artery some fibrosis was found.Before the final, fatal haemorrhage there must havebeen some leakage of blood, and bronchial phy-

yf* comycosis, therefore, must be considered to be apossible cause of haemoptysis.The dense, septate mycelium found in the pus in

the bronchial lumen before death has not beenidentified. Either it is the same phycomycete as wasfound in the infarct or a double mycotic infection

--s was present. Phycomycetes in tissue are not withoutseptae but rarely septate, and it is possible that when

* a phycomycete grows in the peculiar medium ofpus in the bronchus of a diabetic it may developmore septae that it does when it invades tissue.The diagnosis could have been made before death

^ X from the tissue removed at bronchoscopy.oved during

REFERENCESe myceliumA that they Baker, R. D., Seabury, J. H., and Schneidau, J. D., Jr. (1962). Lab.

tination at a Invest., 1i, 1091.Burkitt, D. P., Wilson, A. M. M., and Jelliffe, D. B. (1964). Brit. ined.were found J., 1, 1669.Emmons, C. W., Binford, C. H., and Utz, J. P. (1963). Medical

ons. Mycology, P. 185. Kimpton, London.Kurrein, F. (1954). J. clin. Path., 7, 141.La Touche, C. J., Sutherland, T. W., and Telling, M. (1963). Lancet, 2,

811.Mukerji, S. (1964). Brit. med. J., 2, 1009.

m found in Symmers, W. St. C. (1962). Lab. Invest., 11, 1073.

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